ArticleJournal of molecular neuroscience : MN2014
Evolutionary analysis of voltage-gated potassium channels by Bayes method.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Zebrafish cardiac repolarization does not functionally depend on the expression of the hERG1b-like transcript.Pflugers Archiv : European journal of physiology · 2024Article
- RANKL Impairs the TLR4 Pathway by Increasing TRAF6 and RANK Interaction in Macrophages.BioMed research international · 2022Article
- The Segregated Expression of Voltage-Gated Potassium and Sodium Channels in Neuronal Membranes: Functional Implications and Regulatory Mechanisms.Frontiers in cellular neuroscience · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated potassium channels (VGPCs) are among the most complex families of ion channels. VGPCs are distributed widely among species but their biological roles remain unclear. In this study, the evolution of VGPCs and the functions of ancestral families are determined according to phylogenetic studies. We downloaded 127 genomic data of alpha subunits and 38 genomic data of beta subunits including those from human, rat, mice, Drosophila and Puccinellia tenuiflora. The genetic neighborhood of subfamily genes was determined by neighbor-joining, minimum evolution, maximum parsimony, and Bayes methods. Data was presented as phylogenetic trees. We also detected positive selection sites by site model. New insights into the evolutionary history of the VGPC family are provided. Our assumptions are as follows: (a) KCNH subfamily is likely the most original subfamily in alpha subunit; (b) VGPCs are related to neural and cardiac systems at the earliest time; (c) KCNA4 and KCNF1 may be as ancestors; (d) abnormality in one gene may cause both cardiac and neural diseases; and (e) abnormalities in KCNH6 and KCNQ7 are more likely to cause cardiac diseases.
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Registered trials
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